Immunochip analysis identifies novel susceptibility loci in the human leukocyte antigen region for acquired thrombotic thrombocytopenic purpura

2016 ◽  
Vol 14 (12) ◽  
pp. 2356-2367 ◽  
Author(s):  
I. Mancini ◽  
I. Ricaño-Ponce ◽  
E. Pappalardo ◽  
A. Cairo ◽  
M. M. Gorski ◽  
...  
2017 ◽  
Vol 78 (2) ◽  
pp. 80-87 ◽  
Author(s):  
György Sinkovits ◽  
Ágnes Szilágyi ◽  
Péter Farkas ◽  
Dóra Inotai ◽  
Anikó Szilvási ◽  
...  

2005 ◽  
Vol 76 (1) ◽  
pp. 157-163 ◽  
Author(s):  
Matthew J. Simmonds ◽  
Joanna M.M. Howson ◽  
Joanne M. Heward ◽  
Heather J. Cordell ◽  
Helen Foxall ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Chengappa G. Kavadichanda ◽  
Jie Geng ◽  
Sree Nethra Bulusu ◽  
Vir Singh Negi ◽  
Malini Raghavan

Heritability of Spondyloarthritis (SpA) is highlighted by several familial studies and a high association with the presence of human leukocyte antigen (HLA)-B*27. Though it has been over four decades since the association of HLA-B*27 with SpA was first determined, the pathophysiological roles played by specific HLA-B*27 allotypes are not fully understood. Popular hypotheses include the presentation of arthritogenic peptides, triggering of endoplasmic reticulum (ER) stress by misfolded HLA-B*27, and the interaction between free heavy chains or heavy chain homodimers of HLA-B*27 and immune receptors to drive IL-17 responses. Several non-HLA susceptibility loci have also been identified for SpA, including endoplasmic reticulum aminopeptidases (ERAP) and those related to the IL-23/IL-17 axes. In this review, we summarize clinical aspects of SpA including known characteristics of gut inflammation, enthesitis and new bone formation and the existing models for understanding the association of HLA-B*27 with disease pathogenesis. We also examine newer insights into the biology of HLA class I (HLA-I) proteins and their implications for expanding our understanding of HLA-B*27 contributions to SpA pathogenesis.


Dermatology ◽  
1987 ◽  
Vol 175 (1) ◽  
pp. 10-14 ◽  
Author(s):  
G. Orecchia ◽  
Cuccia Belvedere ◽  
M. Martinetti ◽  
E. Capelli ◽  
G. Rabbiosi

2002 ◽  
Vol 70 (5) ◽  
pp. 1125-1137 ◽  
Author(s):  
Justin P. Rubio ◽  
Melanie Bahlo ◽  
Helmut Butzkueven ◽  
Ingrid A.F. van der Mei ◽  
Michèle M. Sale ◽  
...  

1998 ◽  
Vol 26 (02) ◽  
pp. 191-198 ◽  
Author(s):  
Tatsunori Matsuzaki ◽  
Shosaku Nomura ◽  
Manabu Yamaoka ◽  
Yoshio Ozaki ◽  
Chie Yoshimura ◽  
...  

We performed human leukocyte antigen (HLA) and human platelet antigen (HPA) in patients with Kami-kihi-to-responsive idiopathic thrombocytopenic purpura. The HLA-A2, A61 and Cw1 were significantly increased in responders compared with nonresponders, as were HLA DRB 1 *0901, DRB 1 *1502, and DPB 1 *0501. In contrast, HLA DPB 1 *0201 and DPB 1 *0901 were significantly decreased in responders. The a/b genotype of HPA-2 and a/a genotype of HPA-3 were markedly increased in nonresponders, and anti-GPIb antibody was also increased. These results suggest that HLA, HPA, and anti-GP antibody studies may predict the response of idiopathic thrombocytopenic purpura to Kami-kihi-to.


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